Project Summary Epithelial sheets sit at the boundary of the organism and its external environment. The maintenance of these apical and basolateral domains is essential to the barrier function of epithelia, and the loss of apical-basal polarity is associated with the metastasis of many epithelial cancers. While epithelial sheets were once viewed as largely static assemblies, it is now appreciated that these are dynamic structures that can undergo significant reorganizing and renewal events. Indeed, cell neighbor exchange can be harnessed by developmental processes to effect changes in tissue architecture, and cell intercalation can drive epithelial tissue repair. In the Drosophila embryonic epithelium, individual cells are able to either consolidate cell-cell contacts or direct neighbor exchange movements through the contraction of vertical T1 interfaces and the subsequent resolution of horizontal T3 interfaces. The dominant model in explaining these behaviors has been one in which line tensions that stretch across interfaces direct these changes. However, a number of observations have led us to question this approach. Our central hypothesis is that cell vertices demonstrate radial coupling and that the best explanation of intercalary behaviors will be through a description of the radially-directed force events that lead to vertex movements and subsequent dependent changes in interface lengths. Our data suggests that tricellular vertices slide along cell- cell interfaces to harness radial forces, and would introduce a new area of research on the molecular and biophysical contributions of cell vertices to embryogenesis. Pulsed oscillations in cell area have been found to drive developmental processes in a number of different systems and tissues, but the mechanisms that link these area oscillations to productive tissue shaping events have been unclear. Because of this, we believe vertex sliding through radial force coupling offers a new, fundamental mechanism that may account for this conservation of oscillatory mechanics. We also will examine the structure and oscillation of adhesion complexes that are located at cell vertices, as well as the relationship between actomyosin forces and changes in vertex structure. We believe the proposed studies will provide a fundamentally new vertex-based mechanism that directs cell intercalation through junctional sliding driven by radial coupling.